Author(s): LAKEAS, P., TSITSIMPI, I., DONNELLY, J., COTTER, J., Institution: UNIVERSITY OF OTAGO, Country: NEW ZEALAND, Abstract-ID: 2012

INTRODUCTION:
The Valsalva manoeuvre (VM) is performed during resistance exercise (RE) or daily activities and is a potent cardiovascular stressor. While VM-induced elevations in intrathoracic and intracranial (ICP) pressures have been linked to cerebrovascular and cardiovascular risk, other evidence suggests it may protect cerebral vessels by increasing ICP and thereby limiting cerebrovascular transmural pressure (CVTMP = systolic blood pressure - ICP). Also, the VM is reportedly invoked at ~80% of maximal voluntary contraction (MVC), but this may vary with exercise type, posture, fatigue and active muscle mass. Therefore, this study examined the intensity at which a VM is invoked across exercises and postures, and the effect it has on CVTMP.

METHODS:
Participants were 14 healthy adults (19–27 years, 5 females) with a range of RE background but no history of traumatic brain injury. The exercise intensity at which VM was invoked during 15-s isometric handgrip and squat contractions in standing and supine postures was identified from airflow patterns and concurrent imaging of the right internal jugular vein. The exercises were thereafter performed at intensities 10% below, at, and 10% above the naturally-invoked VM, under both normal breathing and instructed VM conditions, while optic nerve sheath diameter (ONSD) was measured, as a surrogate of increased ICP, using transorbital ultrasound. Exercise, intensity, posture and breathing pattern effects were analysed using repeated-measures ANOVAs.

RESULTS:
The relative exercise intensity at which VM was invoked was higher during handgrip than squats (77 ± 7%. vs 62 ±6%, p<0.001, n2=0.790) but highly variable (ranging handgrip: 57 to 85%, squats: 54-77% MVC), regardless of posture (p=0.500, n2=0.036). The ONSD was 3% larger when supine than seated (p<0.001, n2=0.607), whereas CVTMP was 9% larger when standing (p<0.001, n2=0.765). Invoking a modest VM (30±4 mm Hg) increased ONSD by 9% (p<0.001, n2=0.946), regardless of posture (interaction: p=0.395, n2=0.056), RE (p=0.657, n2=0.021) and exercise intensity (p=0.580, n2=0.041). The VM+RE increased CVTMP (p<0.001, n2=0.759) by 37±10 mm Hg in phase I, 33±7 mm Hg before release (phase IIb), and 41±19 mm Hg in recovery (phase IV), but not during phase IIa (p=0.647) and III (p=0.296), when compared with time-matched normal breathing. These transmural pressures presented a two-fold larger rise when standing than supine (p=0.034, n2=0.259).

CONCLUSION:
These findings challenge the notion that a VM is unavoidable beyond ~80% of MVC and that it protects the cerebral vasculature during RE. The estimated ICP increased during VM+RE only, but was insufficient to counteract the elevations in SBP, particularly during the blood pressure overshoot in recovery (phase IV: Change of SBP +15 vs 41 mm Hg). This resulted in greater CVTMP and therefore vascular wall stress compared with normal breathing.